With Hypertension, I become eclectic. Angiotensin II, not mTOR suddenly becomes the main villain; angiotensin II inhibition is the main treatment and Ariela Benigni is the leading authority on the multiple effects of angiotensin II. This topic was discussed in the section about angiotensin II inhibition. However, this is not outside the world of Blagosklonny as angiotensin II inhibition is part of the Koschei formula and all our references start with Blogosklonny and Koschei. 

mTOR plays a significant role in hypertension as hyperfunctioning vascular smooth muscle cells and increased inflammation plays a major role. Rapamycin can still be expected to block the increased in proinflammatory substances by decreasing messenger RNA used for their production. Furthermore, hypertension causes cardiac hypertrophy and that hypertrophy is blocked by rapamycin. 

Nevertheless, in hypertension, angiotensin II is the main driving force and blocking angiotensin II is the main treatment. In this way, we are similar to traditional medicine. Millions of people are now treated for hypertension with angiotensin II inhibition. We differ slightly form traditional medicine in a few ways.

First, we view blocking angiotensin I receptors in the brain of equal importance as treatment of hypertension. Therefore, we only use angiotensin II inhibitors that cross the blood-brain barrier. This is to protect not only cerebral arteries, but the cerebral microcirculation. Protection of the cerebral microcirculation is about increasing Nitric Oxide synthesis. We also want to decrease chronic inflammation in the brain. Studies have shown that only angiotesin inhibitors that cross the blood-brain barrier protect against development of Alzheimer's disease.

The main drug we like is Candesartan. It crosses the blood-brain barrier, and it doesn't stimulate PPARg, which promotes adipogenesis.

The second difference from traditional medicine, is that we view blocking angiotensin II as not just treating hypertension, but also as acting as an excellent anti-aging drug. 

Blocking Angiotensin I receptors decreases superoxide and increases Nitric oxide. In addition to decreasing hypertension, this has many other beneficial effects including decreasing inflammation, decreasing oxygen free radicals and preserving mitochondria. 

Atherosclerosis is increasingly seen as part auto-immune disease. Oxidized lipoproteins are misinterpreted by pattern-receptors, part of the innate immune system, as foreign invaders. Oxidized lipoproteins then provoke an intense inflammatory reaction. This inflammatory reaction is driven by Angiotensin I receptors and mediated by superoxide. Blocking angiotensin I receptors blocks this reaction.

In hypertension and atherosclerosis, we are dealing with extremely complex and interrelated pathogenesis with very many moving parts. Prevention of the disease process requires treatment on the molecular and cellular level and requires a package of drugs. Statins, metformin, aspirin all play a role in addition to rapamycin and angiotensin II inhibition.